Evidence map›Paper›PMID 28181692›Full record

ArticleJournal of cellular physiology2017

Irisin plays a pivotal role to protect the heart against ischemia and reperfusion injury.

Hao Wang, Yu Tina Zhao, Shouyan Zhang, Patrycja M Dubielecka, Jianfeng Du, Naohiro Yano, Y Eugene Chin, Shougang Zhuang, Gangjian Qin, Ting C Zhao

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
8.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

87 citing papers in PubMed, 140 citations in OpenAlex.

  1. Review
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  4. Irisin deficiency exacerbates cardiac dysfunction and enhances hemorrhage injury in hemorrhage/resuscitation.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
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27 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 2 countries.

Hao WangDepartment of Surgery, Boston University Medical School, Roger Williams Medical Center, Providence, Rhode Island.
Yu Tina ZhaoDepartment of Surgery, Boston University Medical School, Roger Williams Medical Center, Providence, Rhode Island.
Shouyan ZhangDepartment of Cardiology, Luoyang Central Hospital affiliated to Zhengzhou University, Luoyang, Henan, China.
Patrycja M DubieleckaDepartment of Medicine, Alpert Medical School, Brown University, Providence, Rhode Island.
Jianfeng DuDepartment of Surgery, Boston University Medical School, Roger Williams Medical Center, Providence, Rhode Island.
Naohiro YanoWomen and Infants Hospital, Brown University, Providence, Rhode Island.
Y Eugene ChinKey Laboratory of Stem Cell Biology, Institutes of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Shougang ZhuangDepartment of Medicine, Alpert Medical School, Brown University, Providence, Rhode Island.
Gangjian QinFeinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Ting C ZhaoDepartment of Surgery, Boston University Medical School, Roger Williams Medical Center, Providence, Rhode Island.
Roger Williams Medical Center · USBrown University · USChinese Academy of Sciences · CNLuoyang Central Hospital Affiliated to Zhengzhou University · CNNorthwestern University · US

Funding

Histone Deacetylase Inhibition: A Novel Approach to CardioprotectionR01HL089405 · NHLBI · ROGER WILLIAMS MEDICAL CENTER · PI ZHAO, TING C · 2009 to 2020
$3.4M
p38 acetylation: Novel signaling mechanisms and myocardial protectionR01HL115265 · NHLBI · ROGER WILLIAMS MEDICAL CENTER · PI ZHAO, TING C · 2013 to 2016
$1.6M
NHLBI NIH HHS R01 HL089405NHLBI NIH HHS R01 HL115265
6 · The paper itself

Abstract

Irisin, a newly identified hormone, is critical to modulating body metabolism, thermogenesis and reducing oxidative stresses. However, whether irisin protects the heart against myocardial ischemia and reperfusion (I/R) injury remains unknown. In this study, we determine the effect of irisin on myocardial I/R injury in the Langendorff perfused heart and cultured myocytes. Adult C57/BL6 mice were treated with irisin (100 mg/kg) or vehicle for 30 min to elicit preconditioning. The isolated hearts were subjected to 30 min ischemia followed by 30 min reperfusion. Left ventricular function was measured and infarction size were determined using by tetrazolium staining. Western blot was employed to determine myocardial SOD-1, active-caspase 3, annexin V, p38, and phospho-p38. H9c2 cardiomyoblasts were exposed to hypoxia and reoxygenation for assessment of the effects of irisin on mitochondrial respiration and mitochondrial permeability transition pore (mPTP). Irisin treatment produced remarkable improvements in ventricular functional recovery, as evident by the increase in RPP and attenuation in LVEDP. As compared to the vehicle treatment, irisin resulted in a marked reduction of myocardial infarct size. Notably, irisin treatment increased SOD-1 and p38 phosphorylation, but suppressed levels of active-caspase 3, cleaved PARP, and annexin V. In cardiomyoblasts exposed to hypoxia/reoxygenation, irisin treatment significantly attenuated hypoxia/reoxygenation (H/R), as indicated by the reduction of lactate dehydrogenase (LDH) leakage and apoptotic cardiomyocytes. Furthermore, irisin treatments suppressed the opening of mPTP, mitochondrial swelling, and protected mitochondria function. Our results indicate that irisin serves as a novel approach to eliciting cardioprotection, which is associated with the improvement of mitochondrial function.

Indexed as

AnimalsAnnexin A5ApoptosisCardiotonic AgentsCaspase 3Cell LineCytoprotectionDisease Models, AnimalEnzyme ActivationFibronectinsIsolated Heart PreparationMice, Inbred C57BLMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial ContractionAnnexin A5Cardiotonic AgentsCasp3 protein, mouseCaspase 3FibronectinsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition Porep38 Mitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesSod1 protein, mouseSuperoxide Dismutase-1cardioprotectionheartirisinischemia/reperfusion

Identifiers

PMID28181692
PMCPMC5550372
OpenAlexW2586146768

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.